nuclear receptor raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
Reviewed 2026-07-19. Anything still debated is marked as such rather than presented as settled.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516, GW-501516, GW 501516, endurobol | Names vary in research and anti-doping documents. |
| Chemical class | Synthetic PPARδ agonist | Small-molecule nuclear receptor ligand. |
| CAS Registry Number | 317318-70-0 | Identifier commonly associated with GW501516. |
| Appearance | White to off-white powder | Typical for purified research material. |
| Solubility | Low in water; soluble in DMSO and ethanol | Organic solvents are common for laboratory stock solutions. |
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
Cardarine is a common name for GW501516, an investigational compound developed in the 1990s for metabolic conditions. It acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in lipid and energy metabolism. The compound is frequently mislabeled as a selective androgen receptor modulator, or SARM, but its molecular target is different. GW501516 reached early clinical testing before development was discontinued. It has no approved therapeutic use in any country. The name cardarine is not a formal international nonproprietary name.
Regulatory treatment varies, but cardarine is not approved as a medicine. Sports authorities list GW501516 as a prohibited substance, and it is banned at all times under the World Anti-Doping Agency code. Many countries restrict sales for human consumption, while online vendors market it as a research chemical. Such products may lack purity data, and their actual contents can differ from the label. Purchasing or possessing cardarine may carry legal consequences depending on jurisdiction. The compound is not a dietary supplement ingredient in regulated markets.
Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.
Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.
Cardarine has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
== Selected publications == Self, Wesley H.; et al. (2021). "Comparative Effectiveness of Moderna, Pfizer-BioNTech, and Janssen (Johnson & Johnson) Vaccines in Preventing COVID-19 Hospitalizations Among Adults Without Immunocompromising Conditions — United States, March–August 2021". MMWR. Morbidity and Mortality Weekly Report. 70 (38): 1337–1343. doi:10.15585/mmwr.mm7038e1. PMC 8459899. PMID 34555004. Chavez, Miguel A.; Munigala, Satish; Burnham, Carey-Ann D.; Yarbrough, Melanie L.; Warren, David K. (2022). "The Impact of Implementing the Virtuo Blood Culture System on the Characteristics and Management of Patients with Staphylococcus aureus Bacteremia". Journal of Clinical Microbiology. 60 (4): e0226121. doi:10.1128/jcm.02261-21. PMC 9020342. PMID 35291804. S2CID 247453747. Van Belkum, Alex; Burnham, Carey-Ann D.; Rossen, John W. A.; Mallard, Frederic; Rochas, Olivier; Dunne, William Michael (2020). "Innovative and rapid antimicrobial susceptibility testing systems". Nature Reviews Microbiology. 18 (5): 299–311. doi:10.1038/s41579-020-0327-x. hdl:11370/e55ed8f6-6271-4eae-9c45-fc6119f1c851. PMID 32055026. S2CID 211102608. Tahan, Stephen; Parikh, Bijal A.; Droit, Lindsay; Wallace, Meghan A.; Burnham, Carey-Ann D.; Wang, David (2021). "SARS-CoV-2 e Gene Variant Alters Analytical Sensitivity Characteristics of Viral Detection Using a Commercial Reverse Transcription-PCR Assay". Journal of Clinical Microbiology. 59 (7): e0007521. doi:10.1128/JCM.00075-21. PMC 8218754. PMID 33903167.
Bioarchaeology has helped to dispel the idea that life for foragers of the past was "nasty, brutish and short"; bioarchaeological studies reported that foragers of the past were often healthy, while agricultural societies tended to have increased incidence of malnutrition and disease. One study compared foragers from Oakhurst to agriculturalists from K2 and Mapungubwe and reported that agriculturalists from K2 and Mapungubwe were not subject to the lower nutritional levels expected. Danforth argues that more "complex" state-level societies display greater health differences between elites and the rest of society, with elites having the advantage, and that this disparity increases as societies become more unequal. Some status differences in society do not necessarily mean radically different nutritional levels; Powell did not find evidence of great nutritional differences between elites and commoners, but did find lower rates of anemia among elites in Moundville. An area of increasing interest interested in understanding inequality is the study of violence. Researchers analyzing traumatic injuries on human remains have shown that social status and gender can have a significant impact on exposure to violence. Numerous researchers study violence in human remains, exploring violent behavior, including intimate partner violence, child abuse, institutional abuse, torture, warfare, human sacrifice, and structural violence.
=== Diabetes === Januvia (sitagliptin) ($1.3 billion in 2024 revenues) is a dipeptidyl peptidase IV inhibitor for the treatment of type 2 diabetes. In 2013, Januvia was the second largest selling diabetes drug worldwide. It has been popular due in part because unlike many other diabetes drugs, it causes little or no weight gain and is not associated with hypoglycemic episodes. There has been some concern that treatment with Januvia and other DPP-IV inhibitors may be associated with a modestly increased risk of pancreatitis. Janumet ($1.0 billion in 2024 revenues) is a single pill combination drug containing both Januvia and metformin.
One factor that has an important effect on this electrical activity of gonadotrophs is the gonadotropin-releasing hormone (GnRH). GnRH is a hormone released by the hypothalamus, and it is responsible for signaling gonadotrophs to release gonadotropins FSH and LH. GnRH binds to gonadotropin-releasing hormone receptors (GnRHR), which is a G-protein coupled receptor, and signals the oscillation of calcium that hyperpolarizes gonadotropic cell membranes. This oscillation of calcium ions occurs through the resultant signaling cascade of the GnRH binding to the GnRHR in the plasma membrane of the gonadotroph. The G-protein associated with the GnRHR is activated by the binding of GnRH, which results in increased phospholipase C (PLC) activity in the plasma membrane. PLC cleaves phosphatidylinositol-4,5-biophosphate (PIP2) into inositol triphosphate (IP3) and diacylglycerol (DAG) signals. DAG activates protein kinase C (PKC), which phosphorylates proteins, and IP3 binds to IP3 receptors on the membrane of the endoplasmic reticulum (ER). This binding results in the release of intracellular calcium ions stored within the ER. Therefore, this increase in calcium ions signals the synthesis of secretion of FSH and LH in gonadotrophs. Overall, the fluctuation of calcium levels that is activated by the electrical activity and the signaling pathway within gonadotropic cells collectively contribute to the synthesis and release of gonadotropins that will serve an endocrine function in the reproductive system.
Negros was originally called Buglas, an old Hiligaynon word thought to mean "cut off", as the island was thought to have been separated from a larger landmass. It was also known as Mamaylan and Panilougon among Cebuano-speaking Visayans. Among its earliest inhabitants were the aboriginal Ata, one of several Negrito Indigenous Peoples dispersed throughout Southeast Asia that possesses a unique culture. The westernmost portions of the island soon fell under the nominal rule of the Kedatuan of Madja-as based on the neighboring islands of Panay and Guimaras, while the eastern coasts were influenced by the Rajahnate of Cebu from the adjacent island of Cebu.
Sources: en.wikipedia.org
火 (huǒ, fire) e.g.: 烷 (wán, alkane), common for hydrocarbons 酉 (yǒu, ritual wine vessel) e.g.: 酮 (tóng, ketone), common for oxygenated functionalities 艸 (cǎo, grass) e.g. 苯 (běn, benzene, phenyl), common for aromatic compounds and terpenes 肉 (ròu, meat, flesh) e.g. 腙 (zōng, hydrazone), common for nitrogen-containing functionalities Additionally, the mouth radical (口, kǒu) is affixed to characters that are used for their sound only. This occurs often in the transliteration of the names of heterocyclic compounds, (e.g., 吡啶, "bǐdìng", pyridine). These characters are also used for the transliteration of non-chemical terms from foreign languages.
Bauman Moscow State Technical University, founded in 1830, is located in the city center; the university educates 18,000 undergraduate and 1,000 postgraduate students in science and engineering, offering technical degrees.
== Animal models == Knockout mice of GPX4 die at embryonic day 8 and conditional inducible deletion in adult mice (neurons) results in degeneration and death in less than a month. Targeted disruption of the mitochondrial GPX4 isoform (mGPX4) caused infertility in male mice and disruption of the nuclear GPX4 isoform (nGPX4) reduced the structural stability of sperm chromatin, yet both knockout mouse models (for mGPX4 and nGPX4) were fully viable. Surprisingly, knockout of GPX4 heterozygously in mice (GPX4+/−) increases their median life span. Knockout studies with GPX1, GPX2, or GPX3 deficient mice showed that cytosolic GPX4 is so far the only glutathione peroxidase that is indispensable for embryonic development and cell survival. As mechanisms to dispose of both hydrogen peroxide and lipid hydroperoxides are essential to life, this indicates that in contrast to the multiple metabolic pathways that can be utilized to dispose of hydrogen peroxide, pathways for the disposal of lipid hydroperoxides are limited. While mammals have only one copy of the GPX4 gene, fish have two copies, GPX4a and GPX4b. The GPX4's appear to play a greater role in the fish GPX system than in mammals. For example, in fish GPX4 activity contributes to a greater extent to total GPX activity, GPX4a is the most highly expressed selenoprotein mRNA (in contrast to mammals where it is GPX1 mRNA) and GPX4a appears to be highly inducible to changes within the cellular environment, such as changes in methylmercury and selenium status.
== Dynamic features == β-pleated sheet structures are made from extended β-strand polypeptide chains, with strands linked to their neighbours by hydrogen bonds. Due to this extended backbone conformation, β-sheets resist stretching. β-sheets in proteins may carry out low-frequency accordion-like motion as observed by the Raman spectroscopy and analyzed with the quasi-continuum model.
Sources: en.wikipedia.org
While interest in the study of mummies dates as far back as Ptolemaic Greece, most structured scientific study began at the beginning of the 20th century. Prior to this, many rediscovered mummies were sold as curiosities or for use in pseudoscientific novelties such as mummia. The first modern scientific examinations of mummies began in 1901, conducted by professors at the English-language Government School of Medicine in Cairo, Egypt. The first X-ray of a mummy came in 1903, when professors Grafton Elliot Smith and Howard Carter used the only X-ray machine in Cairo at the time to examine the mummified body of Thutmose IV. British chemist Alfred Lucas applied chemical analyses to Egyptian mummies during this same period, which returned many results about the types of substances used in embalming. Lucas also made significant contributions to the analysis of Tutankhamun in 1922. Pathological study of mummies saw varying levels of popularity throughout the 20th century. In 1992, the First World Congress on Mummy Studies was held in Puerto de la Cruz on Tenerife in the Canary Islands. More than 300 scientists attended the Congress to share nearly 100 years of collected data on mummies. The information presented at the meeting triggered a new surge of interest in the subject, with one of the major results being the integration of biomedical and bioarchaeological information on mummies with existing databases. This was not possible prior to the Congress due to the unique and highly specialized techniques required to gather such data.
== History == In 1921, Joslin reported the association of diabetes with hypertension and hyperuricaemia. In 1923, Kylin expanded on this triad. In 1947, Vague observed that upper-body obesity predisposed to diabetes, atherosclerosis, gout and calculi. The term metabolic syndrome began appearing in the late 1950s. In 1967, Avogaro, Crepaldi and coworkers described moderately obese people with diabetes, hypercholesterolemia, and marked hypertriglyceridemia that improved on hypocaloric, low-carbohydrate diets. In 1977, Hans Haller used the term for associations of obesity, diabetes mellitus, hyperlipoproteinemia, hyperuricemia, and hepatic steatosis. The same year, Singer used it for associations of obesity, gout, diabetes, and hypertension with hyperlipoproteinemia. In 1977–1978, Gerald B. Phillips proposed a "constellation of abnormalities" (glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, hypertension) and hypothesised sex hormones as a linking factor. The first comprehensive definition of the metabolic syndrome was given in 1981 by the German researchers Markolf Hanefeld and Wolfgang Leonhardt, Dresden, who defined it as a cluster of obesity, hyper- and dyslipoproteinemia, type 2 diabetes, gout, and hypertension, associated with an increased incidence of atherosclerotic vascular disease, fatty liver disease, and gallstones. In 1988, Gerald M. Reaven's Banting lecture proposed insulin resistance as the underlying factor and coined syndrome X.
One study has found that these steroid-carrier complexes are bound by megalin, a membrane receptor, and are then taken into cells via endocytosis. One possible pathway is that once inside the cell these complexes are taken to the lysosome, where the carrier protein is degraded and the steroid hormone is released into the cytoplasm of the target cell. The hormone then follows a genomic pathway of action. This process is shown in Figure 2 to the right. The role of endocytosis in steroid hormone transport is not well understood and is under further investigation. In order for steroid hormones to cross the lipid bilayer of cells, they must overcome energetic barriers that would prevent their entering or exiting the membrane. Gibbs free energy is an important concept here. These hormones, which are all derived from cholesterol, have hydrophilic functional groups at either end and hydrophobic carbon backbones. When steroid hormones are entering membranes free energy barriers exist when the functional groups are entering the hydrophobic interior of membrane, but it is energetically favorable for the hydrophobic core of these hormones to enter lipid bilayers. These energy barriers and wells are reversed for hormones exiting membranes. Steroid hormones easily enter and exit the membrane at physiologic conditions. They have been shown experimentally to cross membranes near a rate of 20 μm/s, depending on the hormone. Though it is energetically more favorable for hormones to be in the membrane than in the ECF or ICF, they do in fact leave the membrane once they have entered it.
Sources: en.wikipedia.org
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.
No. Cardarine is not a steroid hormone; it targets the nuclear receptor PPARδ. Its classification in anti-doping rules differs from anabolic steroids, though it remains prohibited in sport.
Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.